Cue theme music… Physicians will only use a single, outdated approach, and believe in its exceptional powers to cure everyone. The patient who speaks of suffering is scoffed at, because the thyroid is fine for the doctor used the golden test and miracle cure. “Must be the Internet, the patient doesn’t know what I know,” says the doctor. “Why is my doctor not hearing me?” the patient sighs. She goes home and brings back research, and her doctor tells her not to believe what she reads for his pill works and her TSH is fine. It is not your thyroid, T3 will explode your heart, natural thyroid is impure, TSH is golden and synthetic T4 cures all.

Is it just me or is this whole “thyroid situation” confusing? Seriously? Why does it feel like the medical community is so resistant to listen to patient experience even in the face of a global protest? Current research in the field of endocrinology is supporting the need for treatment options[1], and exposing the flaws of the TSH test.[2] Yet, patient experience reveals that if a patient has lingering symptoms on synthetic thyroxine or with an “in-range” TSH, that physicians say lingering symptoms are “not their thyroid.”[3] How did we get here?

Before science discovered hormones and then created the ability to measure them, the standard for treatment was natural desiccated thyroid.[4] Physicians had no means of testing thyroid hormones, so they treated the patient by watching the patient’s physical presence and symptom report. However, once hormones were identified, synthesized and could be “precisely” measured, the standard treatment moved from a qualitative patient-focus to a quantitative approach of valuing measurements over patient report. The value for technology over patient symptoms report is reflected in current guidelines worldwide for hypothyroidism.

Whether you read the most recently published guidelines for the treatment of hypothyroidism from the American Thyroid Association and American Association of Clinical Endocrinologists[5] or the Royal College of Physicians[6] or almost anywhere worldwide, you will find two over-riding themes in the diagnosis and treatment of hypothyroidism: 1) TSH is the best test to diagnose and treat hypothyroidism 2) The standard treatment is to give the patient enough synthetic T4 so his/her TSH lab value is within an acceptable range. This treatment works for most patients. Easy, right? When is life ever that easy?

As I had stated previously, TSH has been proven in research to not be a reliable indicator of hypothyroidism. Since it is a pituitary hormone, it only tells the medical professional how the pituitary gland is reacting to thyroid hormones that the gland is sensing in its section of the brain. What about beyond the pituitary gland? When you rely on TSH, you are making the following assumptions: 1) the pituitary gland is functioning properly 2) that the amount of thyroid hormone by the pituitary gland is similar to the amount of hormone available to the cells and 3) the available hormone is being used by the cell. Anyone reading this knows that these assumptions obviously cause many exceptions to the TSH rule. There are newer tests such as Free T4 (the amount of T4 in the bloodstream ready to be converted), Free T3 (the amount of useable hormone available for cells) and Reverse T3 (wrongly-converted T3 that is dysfunctional and competes with T3 for cell receptors).[7]

These tests are available, but patients find difficulty getting them run even in the face of lingering hypothyroid symptoms. This impacts patients who are T3 deficient at the cellular level whose TSH never raises with this deficiency. Consequently, too many years pass without effective diagnosis. This also happens to patients who are labeled as “euthyroid” or "in-range" while treated with Synthetic T4 even if they have lingering symptoms. The guidelines do not have precautions for these individuals.

Synthetic T4 is the best treatment for the treatment of hypothyroidism according to the AACE/ATA. These organizations recommends against the treatment of hypothyroidism with animal derived thyroid hormone because there is a lack of research regarding its effectiveness.[8] Wait. How can you determine that synthetic T4 is the best treatment if there are no comparisons? A lack of research is not proof of ineffectiveness. There is compelling research that is demonstrating that there is a need for treatment options.[9] Why are these studies being ignored? There is a collection of over 2,300 counterexamples to T4-only treatment due to their improvement with the addition of T3.[10] Recently, a study found that natural desiccated thyroid is a viable treatment option[11], and another publication that states that physicians ignore chronic symptoms of hypothyroidism.[12] One treatment can never fit all patients.

Even if peer-reviewed, credible studies did not exist, the very nature of thyroid physiology demonstrates that T4 is a storage hormone and not usable on the cellular level. Again, T4 is NOT a useable hormone by the body. It must be converted to T3 for use. If you give a patient a hormone that is not readily useable by the body, you are expecting that the individual’s body will make it useable. How can this assumption be made with checking on this with available laboratory tests?[13]

There are many individuals who have TSH that is in range, and feel good on T4. However, there are many others who, due to stress, low iron levels or other reasons and conditions, do not have the ability to convert T4 to T3. These individuals suffer on synthetic T4-only treatment. It is too difficult for the individual patient to gain access to combination treatment when the need for such options is proven in research. No provisions are made for these individuals in the guidelines.

The vary nature of the word “guidelines” may seem to indicate options and physician discretion, but in societies where medical professionals are brought up on charges (such as those made by the General Medical Council in the UK), or liable for lawsuits for stepping outside of guidelines. Well, then they feel more like rules. For individuals who are not easily diagnosed or treated by TSH values, for those who do not respond well to T4-only treatment, who is going to help them? Provisions in the guidelines must be made to support the research-based decisions of some physicians to treat with T3 containing medications and help restore thyroid patient quality of life. Physicians are not provided the resources to treat those who do respond to “typical” treatment. Instead of extended testing, the patient is prescribed more pharmaceuticals for symptoms, which cause more harm than good. How can T3 therapy be more risky than statins, anti depressants, anti-anxiety meds, heart medications, etc?